Peripheral Immunosenescence and Central Neuroinflammation: A Dangerous Liaison - A Dietary Approach

Magrone, Thea; Magrone, Manrico; Russo, Matteo Antonio; Jirillo, Emilio

doi:10.2174/1871530320666200406123734

Cited by 15 publications

(11 citation statements)

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“…Aging is related with immune senescence and should also be considered as a risk factor for poor prognosis in case of infectious diseases 137 . Moreover, age‐related comorbidities significantly contribute to impair immune system efficiency 138 .…”

Section: Resultsmentioning

confidence: 99%

Worse progression of COVID‐19 in men: Is testosterone a key factor?

et al. 2020

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Background The novel severe acute respiratory syndrome coronavirus (SARS‐CoV‐2) disease 2019 (COVID‐19) seems to have a worse clinical course among infected men compared with women, thus highlighting concerns about gender predisposition to serious prognosis. Therefore, androgens, particularly testosterone (T), could be suspected as playing a critical role in driving this excess of risk. However, gonadal function in critically ill men is actually unknown, mainly because serum T concentration is not routinely measured in clinical practice, even more in this clinical context. Objective To overview on possible mechanisms by which serum T levels could affect the progression of COVID‐19 in men. Methods Authors searched PubMed/MEDLINE, Web of Science, EMBASE, Cochrane Library, Google, and institutional websites for medical subject headings terms and free text words referred to “SARS‐CoV‐2,” “COVID‐19,” “testosterone,” “male hypogonadism,” “gender” “immune system,” “obesity,” “thrombosis” until May 19th 2020. Results T, co‐regulating the expression of angiotensin‐converting enzyme 2 and transmembrane protease serine 2 in host cells, may facilitate SARS‐CoV‐2 internalization. Instead, low serum T levels may predispose to endothelial dysfunction, thrombosis and defective immune response, leading to both impaired viral clearance and systemic inflammation. Obesity, one of the leading causes of severe prognosis in infected patients, is strictly associated with functional hypogonadism, and may consistently strengthen the aforementioned alterations, ultimately predisposing to serious respiratory and systemic consequences. Discussion and conclusion T in comparison to estrogen may predispose men to a widespread COVID‐19 infection. Low serum levels of T, which should be supposed to characterize the hormonal milieu in seriously ill individuals, may predispose men, especially elderly men, to poor prognosis or death. Further studies are needed to confirm these pathophysiological assumptions and to promptly identify adequate therapeutic strategies.

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Section: Resultsmentioning

confidence: 99%

Worse progression of COVID‐19 in men: Is testosterone a key factor?

et al. 2020

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“…The altered foreign presence into brain microenvironment hyper-stimulate local microglia, which in turn produces more pro-inflammatory cytokines. Conversely, the presence of specific inflammatory mediators released from the virus-carrying macrophages may indeed explain an unsolved periodontal or epithelial inflammation due to microorganisms and their endotoxin accumulation [42][43][44][45][46][47][48].…”

Section: Discussionmentioning

confidence: 99%

Oral Microbiota and Immune System Crosstalk: A Translational Research

Ballini

Dipalma

Isacco

et al. 2020

Biology

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Background: Oral pathogens may exert the ability to trigger differently the activation of local macrophage immune responses, for instance Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans induce predominantly pro-inflammatory (M1-like phenotypes) responses, while oral commensal microbiota primarily elicits macrophage functions consistent with the anti-inflammatory (M2-like phenotypes). Methods: In healthy individuals vs. periodontal disease patients’ blood samples, the differentiation process from monocyte to M1 and M2 was conducted using two typical growth factors, the granulocyte/macrophage colony stimulating factor (GM-CSF) and the macrophage colony stimulating factor (M-CSF). Results: In contrast with the current literature our outcomes showed a noticeable increase of macrophage polarization from healthy individuals vs. periodontal patients. The biological and clinical significance of these data was discussed. Conclusions: Our translational findings showed a significant variance between control versus periodontal disease groups in M1 and M2 marker expression within the second group significantly lower skews differentiation of M2-like macrophages towards an M1-like phenotype. Macrophage polarization in periodontal tissue may be responsible for the development and progression of inflammation-induced periodontal tissue damage, including alveolar bone loss, and modulating macrophage function may be a potential strategy for periodontal disease management.

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“…Though the research on COVID-19 is very active globally, the pathogenesis is not yet clearly understood. Previous studies have shown that peripheral immune response and inflammation can cause and exacerbate acute and chronic neuroinflammatory response (Cabrera-Pastor and others 2019; Kempuraj and others 2017; Kempuraj and others 2019a; Kempuraj and others 2019b; Kustrimovic and others 2019; Magrone and others 2020; Skaper and others 2017; Stuve and Zettl 2014). Mast cells are implicated in psychological stress, inflammatory and neuroinflammatory response (Theoharides 2020b).…”

Section: Introductionmentioning

confidence: 99%

COVID-19, Mast Cells, Cytokine Storm, Psychological Stress, and Neuroinflammation

et al. 2020

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Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a new pandemic infectious disease that originated in China. COVID-19 is a global public health emergency of international concern. COVID-19 causes mild to severe illness with high morbidity and mortality, especially in preexisting risk groups. Therapeutic options are now limited to COVID-19. The hallmark of COVID-19 pathogenesis is the cytokine storm with elevated levels of interleukin-6 (IL-6), IL-1β, tumor necrosis factor-alpha (TNF-α), chemokine (C-C-motif) ligand 2 (CCL2), and granulocyte-macrophage colony-stimulating factor (GM-CSF). COVID-19 can cause severe pneumonia, and neurological disorders, including stroke, the damage to the neurovascular unit, blood-brain barrier disruption, high intracranial proinflammatory cytokines, and endothelial cell damage in the brain. Mast cells are innate immune cells and also implicated in adaptive immune response, systemic inflammatory diseases, neuroinflammatory diseases, traumatic brain injury and stroke, and stress disorders. SARS-CoV-2 can activate monocytes/macrophages, dendritic cells, T cells, mast cells, neutrophils, and induce cytokine storm in the lung. COVID-19 can activate mast cells, neurons, glial cells, and endothelial cells. SARS-CoV-2 infection can cause psychological stress and neuroinflammation. In conclusion, COVID-19 can induce mast cell activation, psychological stress, cytokine storm, and neuroinflammation.

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Peripheral Immunosenescence and Central Neuroinflammation: A Dangerous Liaison - A Dietary Approach

Cited by 15 publications

References 0 publications

Worse progression of COVID‐19 in men: Is testosterone a key factor?

Worse progression of COVID‐19 in men: Is testosterone a key factor?

Oral Microbiota and Immune System Crosstalk: A Translational Research

COVID-19, Mast Cells, Cytokine Storm, Psychological Stress, and Neuroinflammation

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